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Stanford researcher: Hallucinatory 'voices' shaped by local culture

The striking difference was that while many of the African and Indian subjects registered predominantly positive experiences with their voices, not one American did. Rather, the U.S. subjects were more likely to report experiences as violent and hateful – and evidence of a sick condition.
The Americans experienced voices as bombardment and as symptoms of a brain disease caused by genes or trauma.
One participant described the voices as “like torturing people, to take their eye out with a fork, or cut someone’s head and drink their blood, really nasty stuff.” Other Americans (five of them) even spoke of their voices as a call to battle or war – “‘the warfare of everyone just yelling.'”
Moreover, the Americans mostly did not report that they knew who spoke to them and they seemed to have less personal relationships with their voices, according to Luhrmann.
Among the Indians in Chennai, more than half (11) heard voices of kin or family members commanding them to do tasks. “They talk as if elder people advising younger people,” one subject said. That contrasts to the Americans, only two of whom heard family members. Also, the Indians heard fewer threatening voices than the Americans – several heard the voices as playful, as manifesting spirits or magic, and even as entertaining. Finally, not as many of them described the voices in terms of a medical or psychiatric problem, as all of the Americans did.

Mental Illness or Mental Injury? | Psychology Today

n fact, we do know from scientific research and the burgeoning field of epigenetics that most of what we call “mental illnesses” are really injuries and not just post-traumatic ones, but chronic and repeated complex trauma. Even our very biological genetic material is affected not only by our own experiences, but those of our ancestors. The field of epigenetics has revived the evolutionary theory of Lamarck[1] from the dustpan of history.

Does dim light make us dumber? -- ScienceDaily

Spending too much time in dimly lit rooms and offices may actually change the brain's structure and hurt one's ability to remember and learn, indicates groundbreaking research by Michigan State University neuroscientists.
The researchers studied the brains of Nile grass rats (which, like humans, are diurnal and sleep at night) after exposing them to dim and bright light for four weeks. The rodents exposed to dim light lost about 30 percent of capacity in the hippocampus, a critical brain region for learning and memory, and performed poorly on a spatial task they had trained on previously.
The rats exposed to bright light, on the other hand, showed significant improvement on the spatial task. Further, when the rodents that had been exposed to dim light were then exposed to bright light for four weeks (after a month-long break), their brain capacity -- and performance on the task -- recovered fully.

A new path into bipolar disorder comes to light -- ScienceDaily

One type of protein produced by IEGs is the so-called Early Growth Response (EGR) proteins, which translate environmental influence into long-term changes in the brain. These proteins are found throughout the brain and are highly produced in response to environmental changes such as stressful stimuli and sleep deprivation. Without the action played out by these proteins, brain cells and the brain itself cannot appropriately respond to the many stimuli that are constantly received from the environment.
Effective neuronal plasticity also depends on neurotrophins, which are regulatory factors that promote development and survival of brain cells. Brain-derived neurotrophic factor (BDNF) is the neurotrophin mostly found in the brain. It has been extensively investigated in BD patients and has been suggested as a hallmark of BD. Indeed, some studies have shown that the levels of BDNF in the serum of BD patients are reduced whenever patients undergo a period of depression, hypomania, or mania. Other studies have shown that regardless of mood state, BD patients present reduced levels of BDNF. Overall, changes in BDNF levels seem to be a characteristic found in BD patients that may contribute to the pathophysiology of the disease.

According to the U.S. Centers for Disease Control and Prevention, each year approximately 16 million individuals in the United States have a major depressive episode. Conventional pharmacological treatments are estimated to produce temporary remission in less than 50 percent of patients, and they are often associated with severe adverse effects. Thus, there is an urgent need for a wider spectrum of novel therapeutics.
Depression is associated with a multitude of pathological processes, including inflammation of the peripheral immune system, a set of biological structures and processes in the lymph nodes and other tissues that protect against disease and abnormalities involving synapses, the structures that permit neurons to pass an electrical or chemical signal to other neurons. However, currently available antidepressants are largely restricted to targeting the systems that regulate serotonin, dopamine, and other related neurotransmitters, and these treatments do not specifically address inflammation and synaptic maladaptations that are now known to be associated with MDD.
Previous research has found that grape-derived polyphenols have some efficacy in modulating aspects of depression, yet the mechanisms of action had largely remained unknown until now. The new study, led by Giulio Maria Pasinetti, PhD, Saunders Professor of Neurology, and a team of investigators from the Center for Integrative Molecular Neuroresilience at the Icahn School of Medicine at Mount Sinai, found that a bioactive dietary polyphenol preparation -- a combination of three grape-derived polyphenol products, including a select Concord grape juice, a select grape seed extract, and trans-resveratrol -- was effective in promoting resilience against stress-induced depression in mice.
Specifically, researchers found that DHCA and Mal-gluc can promote resilience in mouse models of depression by modulating inflammation and synaptic plasticity, respectively. DHCA reduces interleukin 6 (IL-6), a pro-inflammatory substance secreted by T cells and macrophages to stimulate immune response, by epigenetically modulating the non-coding sequence of the IL-6 gene. Mal-gluc modulates histone acetylation of the Rac1 gene and allows transcription activators to access the DNA for increased transcription in the brain, which influences the expression of genes responsible for synaptic plasticity. Researchers also demonstrated that DHCA/Mal-gluc treatment was effective in attenuating depression-like phenotypes in a mouse model of increased systemic inflammation induced by transplantation of cells from the bone marrow of stress-susceptible mice.